Heart failure with preserved ejection fraction: Chronic low-intensity interval exercise training preserves myocardial O2 balance and diastolic function

Kurt D. Marshall, Brittany N. Muller, Maike Krenz, Laurin M. Hanft, Kerry S. McDonald, Kevin C. Dellsperger, Craig A. Emter

Research output: Contribution to journalArticle

36 Scopus citations

Abstract

Heart failure with preserved ejection fraction: chronic low-intensity interval exercise training preserves myocardial O2 balance and diastolic function. J Appl Physiol 114: 131-147, 2013. First published October 25, 2012; doi:10.1152/japplphysiol.01059.2012.-We have previously reported chronic low-intensity interval exercise training attenuates fibrosis, impaired cardiac mitochondrial function, and coronary vascular dysfunction in miniature swine with left ventricular (LV) hypertrophy (Emter CA, Baines CP. Am J Physiol Heart Circ Physiol 299: H1348-H1356, 2010; Emter CA, et al. Am J Physiol Heart Circ Physiol 301: H1687- H1694, 2011). The purpose of this study was to test two hypotheses: 1) chronic low-intensity interval training preserves normal myocardial oxygen supply/demand balance; and 2) training-dependent attenuation of LV fibrotic remodeling improves diastolic function in aortic-banded sedentary, exercise-trained (HF-TR), and control sedentary male Yucatan miniature swine displaying symptoms of heart failure with preserved ejection fraction. Pressure-volume loops, coronary blood flow, and twodimensional speckle tracking ultrasound were utilized in vivo under conditions of increasing peripheral mean arterial pressure and β-adrenergic stimulation 6 mo postsurgery to evaluate cardiac function. Normal diastolic function in HF-TR animals was characterized by prevention of increased time constant of isovolumic relaxation, normal LV untwisting rate, and enhanced apical circumferential and radial strain rate. Reduced fibrosis, normal matrix metalloproteinase-2 and tissue inhibitors of metalloproteinase- 4 mRNA expression, and increased collagen III isoform mRNA levels (P < 0.05) accompanied improved diastolic function following chronic training. Exercise-dependent improvements in coronary blood flow for a given myocardial oxygen consumption (P < 0.05) and cardiac efficiency (stroke work to myocardial oxygen consumption, P < 0.05) were associated with preserved contractile reserve. LV hypertrophy in HF-TR animals was associated with increased activation of Akt and preservation of activated JNK/SAPK. In conclusion, chronic lowintensity interval exercise training attenuates diastolic impairment by promoting compliant extracellular matrix fibrotic components and preserving extracellular matrix regulatory mechanisms, preserves myocardial oxygen balance, and promotes a physiological molecular hypertrophic signaling phenotype in a large animal model resembling heart failure with preserved ejection fraction.

Original languageEnglish (US)
Pages (from-to)131-147
Number of pages17
JournalJournal of Applied Physiology
Volume114
Issue number1
DOIs
StatePublished - Jan 1 2013

Keywords

  • Coronary flow
  • Diastolic heart failure
  • Exercise
  • Fibrosis
  • Hypertrophic signaling
  • MVO
  • Speckle tracking

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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